title: Epithelial-mesenchymal transition and its role in the pathogenesis of colorectal cancer.
abstract: Epithelial-to-mesenchymal transition (EMT) is a collection of events that allows the conversion of adherent epithelial cells, tightly bound to each other within an organized tissue, into independent fibroblastic cells possessing migratory properties and the ability to invade the extracellular matrix. EMT contributes to the complex architecture of the embryo by permitting the progression of embryogenesis from a simple single-cell layer epithelium to a complex three-dimensional organism composed of both epithelial and mesenchymal cells. However, in most tissues EMT is a developmentally restricted process and fully differentiated epithelia typically maintain their epithelial phenotype. Recently, elements of EMT, specially the loss of epithelial markers and the gain of mesenchymal markers, have been observed in pathological states, including epithelial cancers. Increasing evidence has confirmed its presence in human colon during colorectal carcinogenesis. In general, chronic inflammation is considered to be one of the causes of many human cancers including colorectal cancer(CRC). Accordingly, epidemiologic and clinical studies indicate that patients affected by ulcerative colitis and Crohn's disease, the two major forms of inflammatory bowel disease, have an increased risk of developing CRC. A large body of evidence supports roles for the SMAD/STAT3 signaling pathway, the NF-kB pathway, the Ras-mitogen- activated protein kinase/Snail/Slug and microRNAs in the development of colorectal cancers via epithelial-to- mesenchymal transition. Thus, EMT appears to be closely involved in the pathogenesis of colorectal cancer, and analysis refered to it can yield novel targets for therapy.
authors.affiliation: Department of Surgery, The Sixth People's Hospital Affiliated to Shanghai Jiao Tong University, Shanghai, China.
authors.forename: Qing-Chao
authors.initials: QC
authors.lastname: Zhu
authors.forename: Ren-Yuan
authors.initials: RY
authors.lastname: Gao
authors.forename: Wen
authors.initials: W
authors.lastname: Wu
authors.forename: Huan-Long
authors.initials: HL
authors.lastname: Qin
mesh_terms: D002454:Cell Differentiation; D003093:Colitis, Ulcerative / Q000473:pathology*; D015179:Colorectal Neoplasms / Q000473:pathology*; D003424:Crohn Disease / Q000473:pathology*; D004847:Epithelial Cells / Q000378:metabolism; D058750:Epithelial-Mesenchymal Transition; D006801:Humans; D007249:Inflammation; D008648:Mesoderm / Q000166:cytology / Q000378:metabolism; D035683:MicroRNAs / Q000235:genetics; D016328:NF-kappa B / Q000378:metabolism; D050796:STAT3 Transcription Factor / Q000378:metabolism; D015398:Signal Transduction; D051785:Smad Proteins / Q000378:metabolism; D000071250:Snail Family Transcription Factors; D014157:Transcription Factors / Q000378:metabolism; D018631:ras Proteins / Q000378:metabolism
chemical_list: D035683:MicroRNAs; D016328:NF-kappa B; C000604407:SNAI1 protein, human; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D051785:Smad Proteins; D000071250:Snail Family Transcription Factors; D014157:Transcription Factors; D018631:ras Proteins